mTORC1 Activation is not sufficient to suppress hepatic PPAR-a signalling or ketogenesis

we examined if the activation of the anabolic program mediated by the activation of the mTorc1 complex in the fasted state could suppress the robust catabolic programing and enhanced Ppara transcriptional of mice with a liver specific defect in mitochondrial long chain fatty acid oxidation (Cpt2L-/- mice). We found that the activation of mTorc1 in the fasted state was not sufficient to repress Ppara responsive genes or ketogenesis. Overall design: Examination of PPAR-a signalling and ketogenesis through knock-out mouse models. Data collected from chow fed, 24-hour fasted male mouse livers.